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A new mouse gene, Keratin 17n, is mainly found in nail tissue and may explain why mice without Keratin 17 don't have nail issues.

Removing Sprouty genes in mice causes various hormone-related issues but does not increase cancer risk by one year of age.

The Celsr1 gene is crucial for normal hair patterning in mice.

A mouse gene mutation increases the risk of skin cancer.

The Dfl mutation in mice causes poor sebaceous gland function and complete hair loss.

A new keratin 6 type in mice explains why some mice without certain keratin genes still have normal hair and nails.

The hairless mutant gene causes early hair loss and affects skin and thymus development in mice.

Overexpressing CtBP1 in skin cells causes skin and hair problems.

Li2CO3 improved skin disease in a mouse model of Focal Dermal Hypoplasia without toxicity.

Naked-mouse hair lacks certain proteins and has less soluble fibril.

A mutation in the iRhom2 gene causes hairless mice due to abnormal hair follicle development.

Patients with certain FoxN1 gene mutations have severe immune issues but normal skin and hair.

Melanocyte pathology requires keratinocyte hyperplasia and regulation dysfunction.

Hair follicles in the back of the rosette fancy mouse have reversed orientations due to a gene mutation.

Msx2-deficient mice experience irregular hair growth and loss due to disrupted hair cycle phases.

Blocking Wnt signaling in young mice causes thymus shrinkage and cell loss, but recovery is possible when the block is removed.

The wavy coat in NCT mice is caused by multiple genes, including a mutation in the Prss53 gene.

Keratin2-6g is crucial for hair follicle development, with mutations causing cell degeneration and vacuolation.

Loss of the p53 gene alone causes tumors, and losing both p53 and Rb genes speeds up aggressive skin cancer.

MPA increases cancer spread by boosting Eph A2 activity.

Removing the Crif1 gene in mouse skin disrupts skin balance and hair growth.

Hairless mice have longer hair follicles and abnormal structures during the catagen phase.

The p53 protein helps control hair follicle shrinking by promoting cell death in mice.

PRC1 influences skin stem cell development by both turning genes on and off, affecting hair growth and skin cell types.

Researchers created a new mouse model for studying Citrullinemia Type I and similar conditions, showing symptoms and treatment responses like those in humans.

Loss of the p53 gene alone causes tumors, and losing both p53 and Rb genes speeds up aggressive skin cancer.

Mutations in specific keratin genes cause improper hair structure in mice due to faulty keratin protein assembly.

Mice with a changed Hr gene lose and regrow hair due to changes in the gene's activity.

Deleting the MAD2L1 gene in mice led to rapid tumor growth despite chromosomal instability.

The transgene likely activated an oncogene or interrupted a tumor suppressor gene, causing melanoma in mice.